Research lead
A signalling molecule that triggers the immune system may be important in rheumatoid arthritis, according to new research from Imperial College London. Inhibitors could pave the way to more effective arthritis treatments.
The molecule, tenascin-C, triggers the immune system via the same TLR4 switch as an infectious microbe. High levels of tenascin-C in joints may cause the activated immune system to attack the joint, leading to the persistent inflammation of rheumatoid arthritis.
Previous research has shown that mice lacking the TLR4 switch do not show chronic joint inflammation. Kim Midwood, a researcher at the Kennedy Institute of Rheumatology at Imperial College, said it is hoped the findings can be used to develop new therapies that interfere with tenascin-C activation of the immune system, reducing the painful inflammation that is a hallmark of this condition.
In mouse models, mice that can produce tenascin-C have severe joint swelling with bone and cartilage destruction, whereas mice lacking the gene for tenascin-C had no swelling or tissue destruction.
In a subsequent study, the researchers injected tenascin-C into mice joints. This caused the joints to become inflamed and the reaction was dose dependent.
The researchers are now trying to elucidate the precise mechanism by which tenascin-C increases levels of inflammatory molecules in the human joint, and looking for inhibitors.
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